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Background Flavones found in plants display various biological activities, including anti-allergic, anti-viral, anti-inflammatory, anti-oxidation, and anti-tumor effects. In this study, we investigated the anti-tumor effects of flavone, apigenin and luteolin on human breast cancer cells. Methods The anti-cancer activity of flavone, apigenin and luteolin was investigated using the MTS assay. Apoptosis was analyzed by Hoechst 33342 staining, flow cytometry and western blot. Cell migration was determined using the culture inserts and xCELLigence real-time cell analyzer instrument equipped with a CIM-plate 16. Real-time quantitative PCR and western blot were used to determine the signaling pathway elicited by flavone, apigenin and luteolin. Results Flavone, apigenin and luteolin showed potent inhibitory effects on the proliferation of Hs578T, MDA-MB-231 and MCF-7 breast cancer cells in a concentration and time-dependent manner. The ability of flavone, apigenin and luteolin to inhibit the growth of breast cancer cells through apoptosis was confirmed by Hoechst33342 staining and the induction of sub-G1 phase of the cell cycle. Flavone, apigenin and luteolin induced forkhead box O3 (FOXO3a) expression by inhibiting Phosphoinositide 3-kinase (PI3K) and protein kinase B (PKB)/Akt. This subsequently elevated the expression of FOXO3a target genes, including the Cyclin-dependent kinase inhibitors p21 Cip1 (p21) and p27 kip1 (p27), which increased the levels of activated poly(ADP) polymerase (PARP) and cytochrome c . Conclusion Taken together, these data demonstrated that flavone, apigenin and luteolin induced cell cycle arrest and apoptosis in breast cancer cells through inhibiting PI3K/Akt activation and increasing FOXO3a activation, which suggest that flavone, apigenin and luteolin will be the potential leads for the preventing and treating of breast cancer.

The aim was to analyze the association of subfoveal choroidal thickness (SFCT) with age, best-corrected visual acuity, refractive error, and axial length in Taiwan pediatric population. A total of 374 eyes in 187 children were enrolled in this retrospective cross-sectional comparative study, who underwent examinations of best-corrected visual acuity (BCVA), cycloplegic refraction, and axial length (AL). Subfoveal choroidal thickness was assessed utilizing spectral domain enhanced depth imaging optical coherence tomography (EDI-OCT), with measurements taken at the subfovea, defined as the distance from the retinal pigment epithelium to the chorioscleral border. The mean age was 5.6 ± 1.9 years (range 2-16 years). The cycloplegic spherical equivalent refractive error was between + 7.25 and - 15.25 diopters (D) and cycloplegic sphere power was between + 8.25 and - 11.5 diopters (D). The mean SFCT was 299.0 ± 69.80 μm. The mean axial length was 22.87 ± 1.29 mm. In univariate analysis, SFCT had significant positive correlations with spherical equivalent (SE) and sphere power (p < 0.05) and significant negative correlations with age, cylinder power, and axial length (p < 0.05). However, after adjusting in the multivariate regression analysis, spherical equivalent, sphere power and age were not independently associated with SFCT. In multivariate analysis, lower cylinder power and longer axial length have significant correlations with thinner SFCT. The relationship between best-corrected visual acuity and SFCT was not significant in both analyses. This study showed that mean subfoveal choroidal thickness was 299.0 ± 69.80 μm among Taiwanese children. The SFCT was thinner in myopic, longer axial length, and lower cylinder power eyes.

This study aimed to investigate the risk of Alzheimer's disease among patients with age-related macular degeneration and its association with confounding comorbidities. This was a population-based, retrospective cohort study. By accessing data from the National Health Insurance Research Database of Taiwan, we identified 10,578 patients aged 50-100 years who were newly diagnosed with age-related macular degeneration between 2000 and 2012 and 10,578 non- age-related macular degeneration individuals. The comorbidities assessed were osteoporosis, diabetes, cirrhosis, cerebrovascular disease, chronic kidney disease, hypertension, hyperlipidemia, coronary artery disease, and chronic obstructive pulmonary disease. Patients with age-related macular degeneration had a 1.23-fold increased risk of their condition advancing to Alzheimer's disease (aHR = 1.23, 95% CI = 1.04-1.46). The younger patients were diagnosed with age-related macular degeneration, the more likely patients got Alzheimer's disease (50-64 age group: aHR = 1.97, 95% CI = 1.04-3.73; 65-79 age group: aHR = 1.27, 95% CI = 1.02-1.58; 80-100 age group: aHR = 1.06, 95% CI = 0.78-1.45). In addition, there were significantly higher risks of Alzheimer's disease for patients with cirrhosis (aHR = 1.50, 95% CI = 1.09-2.06) in the age-related macular degeneration cohort than in the non-age-related macular degeneration cohort. Patients with age-related macular degeneration may exhibit a higher risk of Alzheimer's disease than people without age-related macular degeneration.

Influenza virus infection is a global public health issue. The effectiveness of antiviral therapies for influenza has been limited by the emergence of drug-resistant viral strains. Therefore, there is an urgent need to identify novel antiviral therapies. Here we tested the effects of 300 traditional Chinese medicines on the replication of various influenza virus strains in a lung cell line, A549, using an influenza-specific luciferase reporter assay. Of the traditional medicines tested, Polygonum cuspidatum (PC) and its active components, resveratrol and emodin, were found to attenuate influenza viral replication in A549 cells. Furthermore, they preferentially inhibited the replication of influenza A virus, including clinical strains isolated in 2009 and 2011 in Taiwan and the laboratory strain A/WSN/33 (H1N1). In addition to inhibiting the expression of hemagglutinin and neuraminidase, PC, emodin, and resveratrol also increased the expression of interferon beta (IFN-β) through Toll-like receptor 9 (TLR9). Moreover, the anti-viral activity of IFN-β or resveratrol was reduced when the A549 cells were treated with neutralizing anti-IFN-β antibodies or a TLR9 inhibitor, suggesting that IFN-β likely acts synergistically with resveratrol to inhibit H1N1 replication. This potential antiviral mechanism, involving direct inhibition of virus replication and simultaneous activation of the host immune response, has not been previously described for a single antiviral molecule. In conclusion, our data support the use of PC, resveratrol or emodin for inhibiting influenza virus replication directly and via TLR-9-induced IFN-β production.

BackgroundHyperinflammation with dysregulated production of galectins and cytokines may develop in COVID-19 or adult-onset Still’s disease (AOSD). Given the similar clinical features in both diseases, it is necessary to identify biomarkers that can differentiate COVID-19 from AOSD. However, the related data remain scarce currently.MethodsIn this cross-sectional study, plasma levels of galectin-3, galectin-9, and soluble TIM-3 (sTIM-3) were determined by ELISA in 55 COVID-19 patients (31 non-severe and 24 severe), 23 active AOSD patients, and 31 healthy controls (HC). The seropositivity for SARS-CoV-2 was examined using an immunochromatographic assay, and cytokine profiles were determined with the MULTIPLEX platform.ResultsSignificantly higher levels of galectin-3, galectin-9, IL-1β, IL-1Ra, IL-10, IFN-α2, IL-6, IL-18, and TNF-α were observed in severe COVID-19 and active AOSD patients compared with HC (all p<0.001). AOSD, but not COVID-19, showed significantly higher IFN-γ and IL-17A compared with HC (both p<0.01). Moreover, active AOSD patients had 68-fold higher IL-18 levels and 5-fold higher ferritin levels than severe COVID-19 patients (both p<0.001). IL-18 levels at the cut-off value 190.5pg/mL had the highest discriminative power for active AOSD and severe COVID-19, with AUC 0.948, sensitivity 91.3%, specificity 95.8%, and accuracy of 91.5% (p<0.005). Multivariate regression analysis revealed IL-18 as a significant predictor of active AOSD (p<0.05).ConclusionActive AOSD patients share features of hyperinflammation and cytokine storm with severe COVID-19 patients but possess a distinct cytokine profile, including elevated IL-18, IL-6, IFN-γ, and IL-17A. IL-18 is a potential discriminator between AOSD and COVID-19 and may significantly predict active AOSD.

Myopia is a highly prevalent refractive disorder. We investigated the effect of diacerein on monocular form deprivation (MFD) in hamsters as a possible therapeutic intervention. Diacerein is an anthraquinone derivative drug whose active metabolite is rhein. Diacerein or atropine was applied to the MFD hamsters, and their refractive error and axial length were measured after 21 days. The refractive error (control: −0.91±0.023, atropine: −0.3±0.08, and diacerein: −0.27±0.07 D) and axial length (control: 0.401±0.017, atropine: 0.326±0.017, and diacerein: 0.334±0.016 mm) showed statistically significant differences between control, atropine-treated, and diacerein-treated MFD eyes. Furthermore, we determined the level of transforming growth factor-beta- (TGF-) β1, matrix metalloproteinase- (MMP-) 2, type I collagen, interleukin- (IL-) 6, IL-8, and monocyte chemoattractant protein- (MCP-) 1 in the retina. Atropine and diacerein suppressed levels of the myopia-related TGF-β1 and MMP-2 while increasing type I collagen expression. They also inhibited the interleukin IL-6, IL-8, and MCP-1 levels. Diacerein reduced the IL-6, IL-8, and MCP-1 expression in ARPE-19 cells. Furthermore, diacerein inhibited inflammation by attenuating the phosphorylation of protein kinase B (AKT) and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) pathway. This suggests that diacerein has a therapeutic effect on myopia and is a potential treatment option.

The formation of foam cells, which are macrophages that have engulfed oxidized low-density lipoprotein (OxLDL), constitutes the first stage in the development of atherosclerosis. Previously, we found that knocking down galectin-12, a negative regulator of lipolysis, leads to reduced secretion of monocyte chemoattractant protein-1 (MCP-1), a chemokine that plays an important role in atherosclerosis. This prompted us to study the role of galectin-12 in atherosclerosis. With that aim, we examined foam cell formation in Gal12‒/‒ murine macrophages exposed to OxLDL and acetylated LDL (AcLDL). Then, we generated an LDL receptor and galectin-12 double knockout (DKO) mice and studied the effect of galectin-12 on macrophage function and atherosclerosis. Lastly, we evaluated the role of galectin-12 in human THP-1 macrophages using a doxycycline-inducible conditional knockdown system. Galectin-12 knockout significantly inhibited foam cell formation in murine macrophages through the downregulation of cluster of differentiation 36 (CD36), and the upregulation of ATP Binding Cassette Subfamily A Member 1 (ABCA1), ATP Binding Cassette Subfamily G Member 1 (ABCG1), and scavenger receptor class B type 1 (SRB1). Consistent with this, galectin-12 knockdown inhibited foam cell formation in human macrophages. In addition, the ablation of galectin-12 promoted M2 macrophage polarization in human and murine macrophages as evidenced by the upregulation of the M2 marker genes, CD206 and CD163, and downregulation of the M1 cytokines, tumor necrosis factor α (TNF- α), interleukin-6 (IL-6), and MCP-1. Moreover, the ablation of galectin-12 decreased atherosclerosis formation in DKO mice. Based on these results, we propose galectin-12 as a potential therapeutic target for atherosclerosis.

Diabetic retinopathy (DR) is a leading cause of vision loss among adults. This study evaluates Optical Coherence Tomography Angiography (OCTA) vessel density (VD) as a marker for DR in diabetes mellitus (DM) patients. An observational study was conducted with 47 type 2 DM patients and 21 healthy controls. OCTA measured superficial and deep retinal VD in the parafoveal region. Statistical analyses, including logistic regression and ROC curve analysis, were used to assess the association between VD and DR presence. Results showed that DM patients had lower parafoveal superficial (46.73 vs. 52.37%, p  = 0.002) and deep VD (50.35 vs. 54.26%, p  = 0.019) compared to controls. Within the DM group, DR patients had lower VD in the superior parafoveal superficial layer ( p  = 0.042) and temporal parafoveal deep layer ( p  = 0.035). ROC analysis identified a cutoff of 51.86% for the temporal deep parafoveal VD, with an AUC of 0.697 ( p  = 0.035) and 81.8% sensitivity for DR discrimination. Reduced VD in the temporal deep parafoveal region is linked to a higher DR likelihood. OCTA-derived VD metrics offer promise for early DR detection and underscore the importance of monitoring vascular changes in DM patients.

Background Poly-D, L-lactic acid is (PDLLA) a new cosmetic filler. We reported the first case of PDLLA-related devastating complication of multiple branch retinal artery occlusion (BRAO). Case presentation A 23-year-old female had sudden blindness after injection of PDLLA at the glabella. After emergency intraocular pressure-lowering medicine, ocular massage, steroid pulse therapy, heparin and alprostadil infusion, and subsequent treatments including acupuncture and 40 sessions of hyperbaric oxygen therapy, her best-corrected visual acuity improved from hand motion at 30 cm to 0.3 within 2 months. Conclusion Although safety of PDLLA was evaluated in animal studies and in 16,000 human cases, it could still cause rare but devastating retinal artery occlusion as in the present case. Proper and immediate therapies could still improve patient’s vision and scotoma. Surgeons should keep in mind the possibility of iatrogenic filler-related retinal artery occlusion.

In recent decades, the impact of air pollution on eye health has been emphasized, but the effect of air pollution on changes in refractive error is still unknown. A comprehensive retrospective cohort study was conducted to address this, utilizing the China Medical University Hospital Clinical Research Data Repository (CMUH-CRDR). It included 4,399 participants aged 6–12 years, with 2,166 females and 2,223 males, who visited the ophthalmology department between 2003 and 2019, ensuring a robust and representative sample. The mean age was 7.04 years (± 2.20), and the change in refractive error was highest in subjects aged between 7 and 9. Cumulative exposure to delicate particulate matter (PM 2.5 ), carbon monoxide (CO), nitrogen oxides (NOx), ozone (O 3 ), and sulfur dioxide (SO 2 ) from the index date to the end of the follow-up was calculated to examine the association between air pollutants and myopia progression. The study found a clear dose-effect relationship, as the change in refractive error progressively increased with higher levels of PM 2.5 , CO, and O 3 , with exposure to the highest levels resulting in a considerably significant change ( p  < 0.05). For every quantile increase in PM 2.5 , CO, NOx, O 3 , and SO 2 , the average change in refractive error decreased by approximately 0.3 D. Among the five air pollutants analyzed, CO had the most significant effect with just one unit increase. PM 2.5 had the most significant impact on refractive error in patients among different age groups (age 5–6, β: − 0.40; age 7–9, β: − 0.47; age 10–12, β: − 0.35). In conclusion, exposure to air pollutants, including PM 2.5 , CO, SO 2 , NOx, and O 3 , increases the risk of myopic progression in children aged between 6 and 12 years old, emphasizing the need for better air quality control measures to protect children’s eye health and prevent myopia progression.